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Cardiogenicshock (CS)is the most feared event following STEMI. We tend to perceive CS as an exclusive complication of STEMI. The incidence is half of that of STEMI, i.e., 2.5-5%. might show little elevation with considerable overlap of left main STEMI vs NSTEMI ) 2.Onset How is CS in NSTEMI different ?
A previously healthy 53 yo woman was transferred to a receiving hospital in cardiogenicshock. So Shark Fin really is just a dramatic representation of STEMI, and can be in any coronary distribution. So this is STEMI, right? This was sent by a reader. and K was normal. Here was the ECG: There is sinus tachycardia.
He was rushed by residents into our critical care room with a diagnosis of STEMI, and they handed me this ECG: There is sinus tachycardia with ST elevation in II, III, and aVF, as well as V4-V6. At first glance, it seems the patient is having a STEMI. ACS and STEMI generally do not cause tachycardia unless there is cardiogenicshock.
The VSR is what is causing the cardiogenicshock! It has been estimated that in the aggregate, they occur at a rate of about 3 per 1000 patients with acute MI, and most of these events occur in patients with STEMI. PIRP is strongly associated with myocardial rupture. PIRP was associated with persistent upright T waves.
Now appears to be in cardiogenicshock." This is ischemia until proven otherwise. However, cardiogenicshock usually takes some time to develop, so it is probably subacute." This can only be due to STEMI. Cardiogenicshock and ACS is an indication for the cath lab, even if you don't think there is OMI.
milla1cf Mon, 04/08/2024 - 18:07 April 8, 2024 — Implantation of the Impella CP micro-axial flow pump in the hours after a heart attack significantly increased the rate of survival at six months among people suffering cardiogenicshock, according to a study presented at the American College of Cardiology ’s Annual Scientific Session.
Clinical Course The paramedic activated a “Code STEMI” alert and transported the patient nearly 50 miles to the closest tertiary medical center. DISCUSSION: The 12-lead EKG EMS initially obtained for this patient showed severe ischemia, with profound "infero-lateral" ST depression and reciprocal ST elevation in lead aVR.
This ECG was read as “No STEMI” with no prior available for comparison. It is true this ECG does not meet STEMI criteria (there is 1.0 The patient has also developed sinus bradycardia, which may result from right coronary artery ischemia to the SA node. Instead we discussed 5 minute delays for the STEMI(+) OMI patients.
The ECG shows obvious STEMI(+) OMI due to probable proximal LAD occlusion. The patient in today’s case presented in cardiogenicshock from proximal LAD occlusion, in conjunction with a subtotally stenosed LMCA. There is no definite evidence of acute ischemia. (ie, The below ECG was recorded.
The axiom of "type 1 (ACS, plaque rupture) STEMIs are not tachycardic unless they are in cardiogenicshock" is not applicable outside of sinus rhythm. In some cases the ischemia can be seen "through" the flutter waves, whereas in other cases the arrhythmia must be terminated before the ischemia can be clearly distinguished.
The baseline ECG is basically normal with no ischemia. You can see in the lead-specific analysis that she "sees" the STD in V5, V5, and II, with STE in aVR as signs of "Not OMI", because subendocardial ischemia pattern is not the same as OMI. In my opinion, I think it looks more like subendocardial ischemia.
This has been termed a “STEMI equivalent” and included in STEMI guidelines, suggesting this patient should receive dual anti-platelets, heparin and immediate cath lab activation–or thrombolysis in centres where cath lab is not available. His response: “subendocardial ischemia. Anything more on history? POCUS will be helpful.”
When the ST vector is primarily posterior, the diagnosis is usually posterior STEMI. Contrary to what Ken stated, the ST vector remains mostly posterior __ What about subendocardial ischemia? Subendocardial ischemia results in ST depression, but unfortunately, and rather mysteriously, it does not localize to the ischemic wall.
Post by Smith and Meyers Sam Ghali ( [link] ) just asked me (Smith): "Steve, do left main coronary artery *occlusions* (actual ones with transmural ischemia) have ST Depression or ST Elevation in aVR?" All are, however, clearly massive STEMI. This is her ECG: An obvious STEMI, but which artery?
There is normal R-wave progression in the precordial leads with no evidence of ischemia. Troponin T peaked at 2074 ng/L (very high, typical of OMI/STEMI). Here the image quality is enhanced using the PM Cardio app. What do you think? The presenting ECG shows SR with narrow QRS complexes. The LV EF was 57% at formal echo.
The patient was brought to the ED as a possible Code STEMI and was seen directly by cardiology. Similarly, STEMI guidelines call for urgent angiography for refractory ischemia or electrical/hemodynamic instability, regardless of ECG findings. But by this time the patient went into cardiogenicshock and passed away.
There is an obvious inferior STEMI, but what else? Why is the patient in shock? Besides the obvious inferior STEMI, there is across the precordial leads also, especially in V1. He was in profound cardiogenicshock. This STE is diagnostic of Right Ventricular STEMI (RV MI). A right sided ECG was not recorded.
The ECG is diagnostic of LAD occlusion (or even left main occlusion possibly), with the classic pattern of RBBB and LAFB with huge concordant STE in V1-V2, I, and aVL, with reciprocal depression in most other leads (and/or a component of subendocardial ischemia pattern). The patient arrived to the ED in cardiogenicshock but awake.
Then the notes mention "cardiogenicshock" but without any reference to a cardiac echo or to a chest x-ray. Cardiologist note says: "Elevated troponin explained by type II MI due to her shock." Trop T now very high, well into the range one sees with a STEMI; very unusual in type II MI. Was there pulmonary edema?
Code STEMI was activated by the ED physician based on the diagnostic ECG for LAD OMI in ventricular paced rhythm. This was several months after the 2022 ACC Guidelines adding modified Sgarbossa criteria as a STEMI equivalent in ventricular paced rhythm). LAFB, atrial flutter, anterolateral STEMI(+) OMI. Limkakeng AT.
Assessment was severe sudden cardiogenicshock. In a series of 18 patients with COVID and ST elevation, 8 were diagnosed with STEMI, 6 of whom had an angiogram and it showed obstructive coronary disease. 12 All STEMI patients had very high cTn typical of STEMI (cTnT > 1.0 They recorded an EC G: New ST Elevation.
This strongly suggests reperfusing RCA ischemia. Troponins, echocardiogram An echocardiogram showed inferobasilar hypokinesis, further supporting a diagnosis of regional ischemia , likely of the area supplied by the RCA. A recent study found that SCAD causes almost 20% of STEMI in young women. There is also a Q-wave in III.
PCI mid LCx So this is an OMI (Occlusion Myocardial Infarction), but not a STEMI Echo: Decreased left ventricular systolic performance, mild/moderate. The patient went into cardiogenicshock and ultimately died of this MI. Angiogram: LM 30% ostial. LAD 80% mid LCx occluded mid (acute infarct lesion) RCA 80% mid. Sandoval Y.
The ECG shows sinus tachycardia, RBBB+LAFB, and signs of anterolateral acute transmural ischemia (most likely due to acute coronary occlusion), with concordant STE in I and aVL, inappropriate STE in V4-6 (though limited a bit by motion, still definite). Near 100% mortality without rapid reperfusion." The ST Elevation is NOT typical.
Whenever there is tachycardia, I am skeptical of OMI unless it has led to severely compromised ejection fracction with cardiogenicshock. Supply-demand mismatch can cause ST Elevation (Type 2 STEMI). Also see these posts of Type II STEMI. Truly, the Marquette 12 SL algorithm correctly identifies this STEMI.
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